Bone mass and especially BMC are highly associated with birth weight. These associations are accounted for mainly by environmental factors that are independent of maternal factors such as gestational age, maternal smoking and nutrition, and are largely mediated by skeletal size and particularly adult height. Birth weight does not appear to be a major influence on the later development of radiographic OA in women.

Genetic factors have a significant contribution to OA at the hip in women and account for approximately 60% of the variation in population liability to the disease.

Objective. Previous case-control studies have shown various degrees of inverse relationship between osteoarthritis (OA) and osteoporosis (OP). The aim of this study was to examine the relationship between radiographic hip OA and bone mineral density (BMD) at the affected and contralateral hips, as well as at more distal sites. We also explored the possibility that this association might be confounded by genetic factors. Methods. Using the discordant twin model to reduce selection bias and adjust for genetic factors, plain pelvic radiographs of white female twins aged >40 years, from the St. Thomas' UK Adult Twin Register, were assessed for radiographic features of hip OA. Overall OA was classified using a 6-point global grading system (Croft). Osteophytes (OPH) and joint space narrowing (JSN) were also examined separately. BMD was measured by dual x-ray absorptiometry at the left hip, lumbar spine, and total body. The association of OA with BMD was assessed using conditional logistic regression. Adjustments were made for body mass index, lifetime physical activity, menopausal status, use of estrogen, and smoking. Results. The analysis included a total of 1,148 women comprising 160 monozygotic and 414 dizygotic twin pairs. The median age of the twins was 53 years (range 40-70). The crude and adjusted odds ratios and 95% confidence intervals for having radiographic features of hip OA were 1.63 (1.06, 2.50) and 1.80 (1.05, 3.12), respectively, per unit difference in standardized BMD of the ipsilateral femoral neck. The presence of OPH, but not JSN, was associated with higher BMD. Twins with hip OPH had 3.5% higher femoral neck BMD than their unaffected cotwins. No clear association was found between hip OA and BMD at the contralateral site, lumbar spine, or total body. Conclusion. This twin study confirms the existence of an inverse relationship between OA and OP at the hip. However, the relationship was localized to the OA-affected hip. The generalized and greater increase in BMD in osteoarthritic subjects seen in previous studies of unrelated populations is therefore likely to be due, in part, to genetic factors shared by hip OA and high bone mass. It also suggests that local changes in bone density may be a component of the disease process in hip OA.

Reduced bone mineral density (BMD), the major risk factor for osteoporotic fracture, has been linked to palmoplantar pustular psoriasis, but no significant studies have examined BMD in chronic plaque psoriasis (CPP). In this study, in-patients with severe CPP had their BMD measured at the nondominant hip and lumbar spine using dual energy X-ray absorbtiometry. Ten male and 10 female Caucasian patients were recruited, with a mean age of 47 years (range 20--71 years). There were no significant differences in BMD between patients and controls. However, patients with psoriatic arthropathy in addition to CPP had a significantly lower mean lumbar spine Z-score (- 1.16) than those without arthropathy (+1.38, P = 0.015). Neither previous nor current treatment with systemic steroids, retinoids or methotrexate significantly affected BMD. We found no evidence that patients with CPP, despite risk factors, have a significantly low BMD, although the subgroup with joint involvement appear be at significantly higher risk of osteoporosis and may therefore require preventative treatment.

QT interval has been determined in 103 monozygotic (MZ) and 198 dizygotic (DZ) female twins. Mean values of corrected QT (QTc) were almost identical for both groups at 413 ms (MZ) and 412 ms (DZ). There was a significant age and environmental effect on QT interval. Keywords: twins; QT; heritability Dominant long QT syndrome causing syncopal attacks and sudden death, has been mapped to several gene loci and functional mutations in these ion channel genes have been identified. 1,2 Although it appears that the likelihood of sudden death from a given cardiac event differs depending on the gene that is mutated to produce LQT, 3 the influence of other background genetic or environmental factors is unclear. Previous studies in a small group of twins indicated a 'significant contribution of genetic effects' on QT interval. 4 Because of current interest in diagnosis and risk evaluation of long QT syndrome we studied QT interval in a large group of MZ and DZ twins.The study cohort was comprised of 301 female Caucasian twin pairs [103 monozygotic (MZ) and 198 dizygotic (DZ) pairs] aged 18-71 years ascertained through a national media campaign in the UK. 5 Zygosity was determined by questionnaire and confirmed with DNA fingerprinting. QT interval and interbeat interval (RR) were measured 'blind' by a trained observer from routine 12 lead ECG traces and the corrected QT (QT c ) was calculated from the equation QT c = QT/√RR.Mean QT c (s.d.) values were 413 (25) ms for MZ and 412 (25) for DZ twins. QT c was significantly correlated with age (r = 0.24, P Ͻ 0.001). Intraclass correlations were larger than zero for both MZ (r = 0.30, P Ͻ 0.001) and DZ twin pairs (r = 0.20, P Ͻ 0.0025) pointing to a significant familial resemblance. The difference between rMZ and rDZ suggests a small heritability. a A = additive genetic influence; D = dominant genetic influence; C = common environmental influence; E (unique) environmental influence; AIC = Akaike's information criteria (these models are described in ref. 5). Note: Apart from the ACE no age model, age was included in all models.with age vs ACE no age: 2 [1] = 29.0, P Ͻ 0.001) and a significant familial resemblance that could be explained either by additive genes (AE vs E: 2 [1] = 11.2, P Ͻ 0.001) or common environment (CE vs E: 2 [1] = 10.7, P Ͻ 0.005). However, the model including age, additive genetic and unique environmental influences gave the most parsimonious explanation of the data, based on the lowest AIC. In this model age explained 6% (95% CI: 2-10) and additive genetic factors (ie, the heritability) 25% (95% CI: 11-38) of the variance, the remaining variance being due to unique environment or measurement error. Thus we find a small heritability for QT c , which in conjunction with unique environmental effects are the major influences on QT variability. The number of unselected twins needed in a genome scan for a power of 80% (␣ = 0.001) to detect a novel QTL explaining 20% of QT c (a very optimistic scenario if total heritability is only 25%) would be Ͼ2500 pairs. A more...